Figure 8.

Proposed model for the regulation of Mad1 and cell fate by miR-125b. On the left, it is shown that high expression of miR-125b downregulates Mad1 as a result of which SAC is transiently activated. This leads to mitotic delay and accumulation of chromosomal abnormalities. The cells fail to maintain themselves and finally undergo apoptotic cell death. On the right, the reverse situation is illustrated. Mad1 levels increase when miR-125b levels are low. As a result, SAC is overridden and premature mitotic exit occurs. This leads to elevated proliferation of cells